Bisphenol A induces apoptosis in central neural cells during early development of Xenopus laevis.

Bisphenol A (BPA), known to be a xenoestrogen, is widely used in industry and dentistry. In the present study, we investigated the effects of BPA on the early development of Xenopus laevis embryos. Stage 6 embryos were exposed to 10-100 microM BPA. Developmental abnormalities were observed when the embryos were exposed to at least 20 microM BPA, with marked developmental abnormalities, such as crooked vertebrae and developmental defects of the head and abdomen, detected in all embryos up to stage 40. Interestingly, apoptosis occurred specifically in central nervous tissue cells of the brain and spinal cord, as assessed by histological analysis. BPA-induced malformations and apoptosis were not observed in embryos exposed to BPA after stage 10. When embryos were exposed to 10 microM 17beta-estradiol (E2), abnormalities were also observed until stage 40. However, the abnormalities induced by BPA and E2 were different and E2 exposure did not induce apoptosis in the central nervous system. Our results indicated that the developmental abnormalities and apoptosis induced by BPA exposure were not inhibited by the addition of E2. In conclusion, we demonstrated that BPA induced marked malformations and specific apoptosis of central nervous system cells during early development of X. laevis embryos, and that these BPA effects appeared to be due to non-estrogenic activities on developmental processes.